Pulmonary Vascular Diseases Flashcards
(199 cards)
1
Q
Right Heart Failure & pulmonary HTN are associated with what?
A
pulmonary emoblism
2
Q
List the 3 components of
Virchow’s Triad?
A
Stasis, endothelial injury, hypercoagulability
3
Q
saddle emboli occur at the bifurcation of what vessel?
A
Right & Left Pulmonary Artery
4
Q
Normal pulmonary BP is clinically defined as ……… of systemic BP.
A
1/8th
5
Q
Pulmonary HTN is clinically defined as ……….. of systemic BP.
A
1/4th
6
Q
Mutation of what protein receptor causes primary pulmonary hypertension and what is the protein’s function?
A
BMPR2; in vascular smooth muscle, inhibits proliferation and promotes apoptosis
7
Q
Pulmonary HTN is morphologically defined by what characteristics?
A
medial hypertrophy of pulmonary vessels & RVH, pulmonary fibrosis, loss of capillary beds
8
Q
Grade 1 PHTN is characterized by what histological features?
A
medial hypertrophy without intimal changes
9
Q
Grade 2 PHTN is characterized by what histological features?
A
Medial Hypertrophy with intimal cellular proliferation
10
Q
Grade 3 PHTN is characterized by what histological features?
A
medial hypertrophy, intimal proliferation & intimal fibrosis
11
Q
Grade 4 PHTN is characterized by what histological features?
A
progressive generalized vascular dilatation; occlusion by intimal fibrosis; fibroelastosis; plexiform lesions
12
Q
Grade 5 PHTN is characterized by what histological features?
A
veinlike branches of hypertrophied muscular arteries; cavernous lesions; angiomatoid lesions
13
Q
Grade 6 PHTN is characterized by what histological features?
A
necrotizing arteritis
14
Q
Group 1 PHTN is associated with what medical conditions?
A
autoimmune diseases
15
Q
Group 2 PHTN is associated with what medical conditions?
A
congenital or acquired heart disease
16
Q
Group 3 PHTN is associated with what medical conditions?
A
Obstructive Sleep Apnea
17
Q
Group 4 PHTN is associated with what medical conditions?
A
recurrent thromboemboli
18
Q
Describe the pathogenesis of Goodpasture syndrome?
A
circulating autoantibodies against a3 chain of collagen IV
19
Q
what are the pulmonary histological findings of GP syndrome?
A
red-brown consolidation; focal necrosis of alveolar walls assoc. w/ intra-alveolar hemorrhages; hemosiderin-laden macrophages; in later stages: thickening pulmonary fibrosis, type II pneumocyte & alveolar space hyperplasia
20
Q
what are the renal histological findings of GP syndrome?
A
focal proliferative glomerulonephritis
21
Q
What are the clinical hallmarks of idiopathic pulmonary hemosiderosis?
A
cough, hemoptysis, anemia
22
Q
What are the histological hallmarks of idiopathic pulmonary hemosiderosis?
A
hemosiderin laden macrophages in alveolar spaces
23
Q
what are the histological hallmarks of granulomatosis with polyangiitis?
A
necrotizing granulomas in URT; granulomatous vasculitis of small to medium sized vessels; focal crescentic glomerulitis
24
Q
Fibromuscular Intimal Hyperplasia is driven by what biological response and what types of vessels does it affect?
A
inflammation or mechanical injury; muscular large arteries
25
Monckeberg medial sclerosis affects which vascular layer?
Tunica Media; "pipestem" appearance on x-ray
26
Hyaline arteriolosclerosis is defined as what and is associated with which clinical conditions?
proteins leaks into vessel wall; commonly seen with cases of essential HTN & DM
27
Hyperplastic arteriolosclerosis is defined as what and is associated with which clinical conditions?
thickening of vessel wall by hyperplasia of smooth muscle; commonly seen with malignant HTN and appears as an "onion-skinning" pattern under the microscope
28
arteriolosclerosis affects which type of vessels?
small arteries & arterioles
29
Atherosclerosis affects which type of vessels?
tunica intima
30
what is the definition of an Atheroma?
raised focal lesion within the intima; consists of cholesterol covered by a fibrous cap
31
List the 3 major components of atheromas?
cells: SM, macrophages, t-lymphocytes; ECM: collagen, elastic fibers, proteoglycans; Intracellular & extracellular lipid
32
Systemic inflammation is indicated by which biomarker?
C-reactive protein (CRP)
33
monocytes & t-lymphocytes bind to which receptor on dysfunctional endothelial cells?
VCAM-1
34
VSMC recruitment to the tunica intima is mediated by which factors?
PDGF & FGF
35
What components involved in the mediation of endothelial dysfunction can destabilize a plaque?
macrophages; high microvessel density; thin fibrous cap; presence of intraplaque hemorrhage; cap rupture; superimposed thrombus; large lipid core; increased levels of MMPs; SM hypoplasia
36
Describe the 6 stages of atherosclerosis progression?
I: isolated macrophage foam cells; II: intracellular lipid accumulation; III: II + extracellular lipid accumulation; IV: II + more severe III; V: lipid core & fibrotic layer, calcific; VI: hematoma, hemorrhage, thrombosis
37
Aneurysm arise from which vessel layer & what are the physiological consequences?
thickened tunica intima means less O2 diffusion to other layers of the vessel wall causing atrophy of media and adventitia layers
38
Define Angina pectoris.
uncomfortable chest sensation produced by myocardial ischemia
39
Define stable Angina.
transient angina precipitated by exercise and relieved by rest; oxygen demand exceeds available blood supply
40
Define unstable angina.
increased frequency and duration of episodes produced at rest; oxygen demand unchanged
41
Define Variant Angina.
chest discomfort at rest due to coronary artery spasm rather than increased myocardial oxygen demand
42
Tn-I & Tn-2 begin to rise after how much time after an MI and peaks when and remains elevated for how long?
2 - 4 hrs.; peaks at 24 hr.; remain elevated for 7-10 days after MI episode
43
CK-MB begin to rise after how much time after an MI, peaks when, & and returns to normal after how much time?
rises within 4-8 hrs.; peaks at 24 hr. & returns to normal by 72 hrs.
44
Why is CK-MB a more useful biomarker for determining re-infarctions than troponins?
B/C levels should return to normal after 72 hrs. from initial episode while troponins take several days to go back down to normal
45
What MI changes can be seen 0-30 min after initial episode?
nothing
46
what MI changes can be seen b/t 30 min-4 hrs. after initial MI episode?
wavy fibers
47
what MI changes can be seen b/t 4 & 12 hrs. after initial MI episode?
start of coagulative necrosis, edema, & hemorrhage; focal mottling
48
what MI changes can be seen b/t 12 & 24 hrs. after initial MI episode?
pyknosis, myocyte hypereosinophilia, neutrophil infiltrate; contraction band necrosis; dark mottling
49
what MI changes can be seen after 1-3 days following a MI episode?
loss of nuclei, interstitial infiltration of neutrophils, yellow-tan infarct center
50
what MI changes can be seen 3-7 days following an MI episode?
yellow-tan center; phagocytosis of dead cells by macrophages
51
what MI changes can be seen 7-10 days after an MI episode?
maximal yellow tan w/ depressed red-tan margins; early granulation tissue
52
what MI changes can be seen 10-14 days after MI episode?
red-grey infarct borders; mature granulation tissue w/ angiogenesis, formation of collagen
53
what MI changes can be seen 2-8 weeks following an MI episode?
grey-white infarction scar; increased collagen density, decreased cellularity & vascularity
54
what MI changes can be seen after 2 months following an MI episode?
scarring complete; all that remains is a dense collagen scar where the infarct occured
55
What are the physiological consequences of vascular ischemia?
decreased oxidative phosphorylation assoc. w/ decreased ATP production; decreased function of Na+ pump; subsequent influx of H20 & Na+ causing cells to swell
56
Describe the pathogenesis of contraction bands.
Form in cells where ATP is greatly diminished or absent; such is the case for ischemia induced MIs which causes hypercontraction of myocyte sarcomeres leading to a tetanic state; assoc. w/ reperfusion injury
57
Arrhythmias assoc. w/ SA & AV Nodes involve which coronary artery?
RCA
58
Arrhythmias assoc. w/ Bundle of his involve which artery?
LAD
59
What are the clinical symptoms & signs assoc. w/ pericarditis?
Symptoms: sharp pain aggravated by inspiration relieved by leaning forward or sitting up, Hypotension assoc. w/ pulsus paradoxus; Signs: friction rub on PE, Water bottle configuration of radiography, EKG findings: ST segment elevation & PR segment depression
60
What is the pathogenesis of Dressler's syndrome?
autoantibodies directed against damaged pericardial antigens; autoimmune induced fibrinous pericarditis
61
What can cause myocardial rupture & how many days after an MI does it usually occur?
b/t 3-7 days after MI episode; myocardium weakened by coagulative necrosis, neutrophilic infiltrate, & lysis of myocardial connective tissue
62
Describe different pathogenesis that can lead to rupture of the ventricular free wall.
Cardiac Tamponade: compression of heart by a fluid-filled pericardium; Kussmaul sign: paradoxical rise in JVP on inspiration indicative of limited filling of the right ventricle
63
What is a false aneurysm?
when the epicardium & pericardium form an adherent wall
64
What is a true ventricular aneurysm?
narrowing of ventricular wall that budges outward into the pericardial space
65
What is the most common cause of a papillary muscle rupture?
occlusion of RCA leading to ischemia of posterior LV 1/3 septum where posterior leaflet of mitral valve attaches
66
what are the most common causes of rupture to the ventricular septum?
Lt. to rt. shut; JVD; pedal edema; right sided heart failure; assoc. w/ LAD coronary artery thrombosis
67
List the components of metabolic syndrome?
large waistline; high level of TGs; Low HDL; high LDL; HTN; glucose intolerance
68
what is the precursor for bile salts?
cholesterol
69
How is cholesterol eliminated from the body?
via feces
70
Lipids have poor solubility; what does the body due to increase solubility?
hydroxylation & carboxylation increase solubility of bile salts
71
What are the 2 main primary bile acids synthesized by the body and makes makes them primary bile acids?
cholic acid; chenodeoxycholic acid; primary b/c they are produced in the liver
72
What are the 2 main secondary bile acids synthesized by the body and what makes them secondary bile acids?
deoxycholic acid; lithocholic acid; secondary b/t they are produced from bacterial enzymes in the small intestine from primary bile acids
73
Why are secondary bile acids more likely to be excreted than primary?
they are less soluble due to loss of hydroxyl group and therefore harder to reabsorb
74
Describe the biological process of bile acid conjugation.
addition of an amino acid to the carbon 24 carboxylate: the two main ones are glycine and taurine
75
conjugated bile salts have a lower pKa than physiological pH; therefore what form will be more prevalent in the small intestine where the pH is 6?
higher percentage of ionized form
76
Where in the colon does bile acid reabsorption take place?
Ileum
77
Describe the pathogenesis of choleithiasis.
cholesterol gallstone disease due to imbalance of cholesterol, phospholipids, & bile salts
78
what is another name for Type I hyperlipoproteinemia?
Familial lipoprotein lipase deficiency
79
what is another name for Type IIa Hyperlipoproteinemia?
familial hypercholesterolemia
80
what is another name for Type IV Hyperlipoproteinemia?
familial hypertriacylglycerolemia
81
What are some common risk factors for DVT?
Immobility; H/o of thromboembolic disease; use of estrogen; pregnancy; neoplasia; CHF; MI; obesity
82
Why is smoking while taking oral contraception not advised?
use of estrogen already increases risk of PE & DVT 6x from baseline and smoking will only increase this factor
83
Why is pregnancy considered a risk factor for thromboembolic disease?
uterine enlargement promotes venous stasis of LEs; thrombocytosis; increased platelet adhesiveness; release of thromboplastin at time of placental separation
84
What types of neoplasia are assoc. w/ increased risk of TED?
lung; pancreas; breast; GI; GU
85
Trousseau sign of malignancy indicates what and in what veins can this sign be seen?
indicates migratory thrombophlebitis in superficial veins
86
what kinds of deficiencies can increase risk of TED?
Antitrhombin III; Protein C (extremely rare); protein S; plasminogen activators
87
Why do mutations of Factor V Leiden increase risk of TED?
results in factor V being more resistant to cleavage by protein C
88
What is the clinical presentation of PE?
dyspnea (most common); angina; anxiety; syncope; cough; hemoptysis (not commom)
89
What are the typical PE findings assoc. w/ PE?
tachypnea; tachycardia; fever; focal crackles; rarely wheezing & cyanosis
90
Pulmonary infarction is more commonly assoc. with what preexisting conditions?
LVF; mitral stenosis; COPD
91
What is the gold standard for diagnosing DVT?
Venous ultrasonography; venography
92
D-Dimer testing can only be used to rule out DVT if what is low and negative?
pretest probability of PE
93
what is the gold standard for diagnosing PE?
pulmonary angiogram
94
what is the drug of choice for prophylaxis of venous thromboembolism?
low molecular weight heparin
95
RVF is commonly assoc. w/ what type of PE?
submassive PE with SBP > 90 mmHG
96
What type of PE is assoc. w/ hemodynamic compromise & shock?
massive PE; SBP < 90 mmHg
97
Stable Angina is assoc. w/ what % of vessel occulsion?
70%
98
Stable Angina is associated w/ low V/Q ratio; how does this affect Oxygen supply and demand?
decreased O2 supply and increases O2 demand
99
what are the 4 factors that when increased will also increase O2 demand?
HR; inotropy; preload; afterload
100
What is Monday Disease?
seen in pts. that work in nitrate factories
101
ACS encompasses
Unstable Angina; NSTEMI; STEMI
102
unstable angina occurs when there is a ......% occlusion of coronary blood vessels.
90%
103
Unstable angina is usually assoc. w/ what kind of MI?
NSTEMI
104
STEMIs are assoc. w/ what % of artery occlusion?
100%
105
Other than EKG findings, how else can unstable Angina w/ MI be distinguished from unstable angina with no MI?
NSTEMIs and STEMIs are going to indicate elevated plasma levels of Troponin & CK-MB
106
what factors are used to calculate level of risk for recurrent CVD episodes?
History; EKG; Age; secondary risk factors; troponin
107
Why should fibrinolysis be avoided for pts. w/ NSTEMIs?
This is basic fluid mechanics; fluids will naturally flow through routes of the least resistance; in the case of stenosis, the blood vessel is already narrowed so fluid is not going to want to naturally flow into the occluded artery in any case
108
Why is fibrinolysis indicated for STEMIs and not NSTEMI?
the fluid mechanics do not change; so blood will still want to flow away from the occluded artery; however if the vessel was 100% occluded which is the case in STEMIs, then even a partial opening will at least stabilize the pt. temporarily until an angioplasty can be done
109
what are absolute CIs for Fibrinolysis treatment of occluded arteries?
cerebral vascular lesion; ICH; intracranial neoplasm; ischemic stroke within last 3 months; pre-existing bleeding disorders; head trauma
110
Ventricular arrhythmias induced by MI complications typically occur how long after the MI?
0-24 hrs.
111
Pericarditis typically presents as an MI complication how long after the MI?
1-3 days
112
Dressler syndrome can occur how many days after an MI?
2 weeks to several months
113
what does the ASCVD risk calculator assess?
probability of a CVD event in a 10 yr. period
114
what is the recommended daily sodium intake?
2300 mg/day
115
what is the most common culprit of PAD?
atherosclerosis
116
What is the typical clinical presentation for myalgia induced PAD?
claudication that is relieved by rest; impaired wound healing of the LEs
117
What are the main symptoms of spinal stenosis induced claudication?
positional relief; paresthesia; radiculopathy
118
If a pt. is complaining of claudication in their popliteal fossa, where is the vessel obstruction most likely located?
femoral artery
119
what is the qualitative definition of ABI?
ratio of ankle pressure to systemic pressure
120
how is ABI calculated?
measure brachial, dorsalis pedis, & posterior tibia BPs; then take the highest BP for the LE and divide by the brachial BP
121
What is the clinical significance of the ABI?
The ABI gives you an indication of how severe the atherosclerosis is; the lower the ratio the more severe the PAD
122
what would be the next step for a pt. w/ an ABI < 0.9?
Imaging w/ CTA or MRA; DSA is gold standard b/c it is the most sensitive but more invasive and very expensive
123
What is commonly seen in pts. w/ an ABI < 0.4?
ischemic rest pain & tissue loss
124
what does an ABI > 1.3 indicate?
pt. has calcified arteries rendering the ABI invalid for diagnosing PAD
125
What are the main clinical signs of Acute limb ischemia?
LE palpitations; pallor; pain; paresthesis; paralysis; poikilothermia
126
What are the main clinical signs for chronic Limb-threatening ischemia?
ABI < 0.4; rest pain; ulcers & gangrene in LEs
127
What are the main differences b/t CAD & PAD?
CAD is assoc. w/ STEMI & NSTEMI; PAD is assoc/ w/ gangrene rest pain & claudication
128
What is another term for Aortoiliac occlusive disease?
leriche syndrome
129
what are the clinical signs of leriche syndrome?
claudication of buttock & thigh; decreased femoral pulses; Erectile dysfunction
130
what is the most common culprit of a stroke?
carotid atheroembolus
131
What is the clinical presentation for Transient Ischemic Attack?
focal cerebral deficits (depending on which artery in circle of Willis is occluded); episode lasts 2-15 min; unilateral motor, sensory loss and sometimes aphasia and dysarthria
132
If a pt. presents with symptoms of transient monocular blindness what branch of the IC is most likely occluded?
ophthalmic division
133
How is carotid stenosis screened?
duplex U/S
134
What is May-Thurner Syndrome?
compression of common iliac vein by common iliac artery
135
Why are pts. with a h/o DVT at increased risk for CVI & post-thrombotic syndrome?
DVT can damage the vessel walls which will promote coagulation & inflammation leading to endothelial damage
136
where are venous and arterial ulcers in LEs most commonly located?
venous ulcers: 2-3 above medial malleolus and appear more fibrous; arterial ulcers: will appear more gangrenous & found in distal toes and on top of bony prominences
137
what are primary causes of lymphedema?
milroy disease (LE edema in subQ and extensive ST hypertrophy); hypoplastic toenails; praecox (extensive ST swelling); isolated dorsal foot swelling
138
what are common secondary causes of lymphedema?
infection (W. bancrofti); trauma; prior surgery; lymph node dissection; radiation; cancer
139
What are the the clinical signs of Stage 1 lymphedema?
pitting that is relieved by elevation
140
what are the clinical signs of State 2 lymphedema?
not fully relieved by elevation; pitting is variable
141
what are clinical signs of State III lymphedema?
elephantiasis w/ severe fibrosis, warty overgrowths; fat deposition; no pitting
142
Lymphangiosarcoma is most commonly found in what region of the body?
UEs
143
Unlike atherosclerosis, which only affects the tunica intima, aneurysms affect all 3 vascular layers; describe the different types in your own words.
fusiform: the entire perimeter of the vessel is swollen; saccular: only a portion of the vessel perimeter is affected; eccentric: looks like a round bud coming off of the main vessel
144
What is a pseudoaneurysm?
false aneurysm b/c only the tunica media & intima are affected; adventitia remains intact
145
what are risk factors for aneurysm?
chronic use of tobacco products; HTN, AS, diseases of chronic inflammation
146
how are aneurysms formed in the blood vessel?
form when there is a reduction of strength and elasticity of the tunica media
147
what can cause the tunica media to loose its elasticity?
leiomyo hypoplasia; increased proteinase activity; destruction of ECM; chronic inflammation
148
what is the most important risk factor for thoracic aortic aneurysms?
HTN!!!!!!!!!!!!
149
What congenital diseases are accoc. w/ increased risk for TAA?
Marfan syndrome (defective fibrillin); EDS Type IV (defect of type III collagen); Loeys-Dietz (defective TGF-beta receptor); bicuspid aortic valve heart defect
150
what infectious agents can cause TAA?
syphilis, S. Aureus
151
what are other risk factors for TAA?
aortitis; chest trauma
152
what is the most common place for traumatic aortic injury (TAI)
aortic isthmus just distal to the left subclavian artery
153
why is TAI a pseudoaneurysm?
does not affect the tunica adventitia
154
why is the aortic isthmus the most common location for TAI?
Isthmus is a latin term for a narrowing making this part of the aorta intrinsically weaker; this is also a transition zone for ascending and descending aorta; shear stress from the ligamentum arteriosum can also cause this region to be weaker
155
what is the most common cause of death for pts. w/ marfan syndrome
aortic dissection/rupture
156
what is the most common cause of death for Type IV EDS?
arterial rupture
157
What are clinical distinctions that can be made b/t Marfan & Loeys-Dietz syndromes?
bifid uvula; hypertelorism; cervical spine deformity; these are all unique to LDS and typically not seen in pts. w/ marfan
158
what is the physiological consequence of having a bicuspid Aortic valve instead of a tricuspid one?
decreased valve cross-sectional area; this will increase the aortic pressure and cause increased wall stress; result is overdilation of aorta and more susceptibility for developing a TAA
159
syphilis affects what part of the aorta?
vasa vasorum
160
obliterative endarteritis causes what biological response?
inflammation and tissue proliferation leading to occulsion
161
TAA can be categorized into what 3 subtypes?
Ascending Thoracic Aorta; Aortic Arch & Descending Thoracic Aorta
162
A TAA in the ATA can lead to what physiological consequences?
aortic regurgitation leading to HF
163
what are clinical signs of a TAA in the coronary artery of the AA?
myocardial ischemia or infarction
164
what are clinical signs of a TAA in the superior vena cave portion of the AA?
JVD, facial and UE edema
165
what are clinical signs of a TAA in the pulmonary artery portion of the AA?
PE-like symptoms
166
what are the clinical signs of a TAA in the airway portion of the AA?
dyspnea, cough, wheezing
167
If the left recurrent laryngeal nerve is being affected by a TAA in the AA, what is the most common sign?
hoarseness
168
what would be the main CC of a TAA in the DTA?
back pain
169
What are signs of a TAA that can be seen on a CXR?
widened mediastinum; aortic knob hypertrophy; trachea deviation
170
TAAs in the DAT are susceptible to thrombus formation; where do these thrombi typically emolize to?
disal regions of the body such as the renal arteries and arteries in the LEs
171
Rupture of the TAA can lead to what physiological conseqneces?
acute pericardial tamponade
172
What would be the physiological consequences if the TA were to rupture?
pleural effusion; hemorrhagic shock; respiratory failure
173
what is the main culprit of abdominal aortic aneurysm?
AS!!!!!!!!!!!!!
174
what is the most affected blood vessel by AS?
abdominal aorta
175
why is the infrarenal aorta the most common site for AAAs?
lacks a vasa vasorum of its own and therefore relies on diffusion from the tunica intima of the Abdominal aorta for oxygen and nutrients
176
what are the histological hallmarks for inflammatory AAAs?
dense, periaortic fibrosis of the tunica adventitia
177
Mycotic AAAs are caused by what?
bacterial infections: S. Aureus, Salmonella (often assoc. w/ gastroenteritis), S. epidermidis (usually on occur if an AAA already exists)
178
What is a clinical hallmark for AAA on PEs?
pulsatile abdominal masses
179
What is the most common diagnostic tool for AAA?
Ultrasound
180
Tearing of which two layers defines an aortic dissection?
tearing of the tunica intima & media from the aortic wall
181
The new cavity that forms from the result of an aortic dissection is referred as what?
false lumen
182
what is the definitive diagnosis for AD?
CTA
183
What would be the signs of a clinical vignette for a pt. w/ aortic dissection?
sudden onset of severe chest pain described as "tearing" with radiation to the back
184
Describe a DeBakey I AD in your own words?
dissection of the TAA that propagates to all portions of the TAA perimeter
185
Describe a DeBakey II AD in your own words?
dissection of the TAA isolated to one region in the vessel
186
describe a DeBakey III AD in your own words?
AD of the DTA or the AAA after leaving the left subclavin artery
187
what are clinical signs of malperfusion syndrome related to an AD that spreads to the coronary arteries?
myocardial ischemia or MI
188
what are clinical signs of malperfusion syndrome related to an AD that spread to the carotid arteries?
TIA, stroke, dysphasia, neurologic deficits
189
what are clinical signs of malperfusion syndrome related to an AD that spread to the mesenteric arteries?
abdominal pain, mesenteric ischemia
190
what are clinical signs of malperfusion syndrome related to an AD that spread to the renal arteries?
acute renal failure, oliguria or anuria
191
JVP will be reduced when this happens?
hypovolemia
192
the diaphragm is better for detecting what kind of sounds?
high-pitched; S1, S2, S4
193
the bell is better for detecting what kind of sounds?
low-pitched; S3; mitral stenosis
194
how can you discern if a murmur is assoc. w/ systole or distole?
murmur is also heard with auscultation of the carotids
195
A cardiomyopathy of the aortic & pulmonary valves are most likely to be heard in which regions of the chest?
base of the heart B/L 2nd ICS
196
cardiomyopathies of the AV valves can be heard where on the chest?
tricuspid valve: sternal aspect of the left apex; bicuspid (mitral): posterolateral of tricuspid area no further than the 5th ICS (left midclavicular line)
197
What are clinical indications of a palpable PMI that is sustained or stuck out?
LVH
198
What are clinical indications of a palpable PMI that is diffusely distributed?
CHF; dilated cardiomyopathy
199
Cardiac sympathetic innervation is in what vertebral levels? And parasympathetics?
T1-T5 for sympathetic innervation; Parasympathetic: right vagus for SA node & left vagus for AV node
